What is the most likely cause of a 38-year-old male's increasing shortness of breath (SOB) over 5 days, with a history of recent respiratory infection, low oxygen saturation (hypoxemia), and normal arterial blood gas (ABG) parameters except for low partial pressure of oxygen (Po2)?

Acute Respiratory Distress Syndrome (ARDS) Following Respiratory Infection

The most likely diagnosis is D. Pulmonary edema, specifically non-cardiogenic pulmonary edema from ARDS, which presents with severe hypoxemia (PO2 5 kPa, SpO2 78%) with preserved ventilation (normal pH, PCO2, HCO3) and tachypnea—the hallmark features of Type 1 respiratory failure from ventilation-perfusion mismatch and intrapulmonary shunting. 1

Clinical Reasoning

Why ARDS (Pulmonary Edema) is Correct

The patient's presentation is pathognomonic for ARDS developing after respiratory infection:

• The 5-day timeline from respiratory infection to progressive dyspnea matches the typical ARDS development window of 1-5 days after the initial insult 1
• Severe hypoxemia (PO2 5 kPa/38 mmHg, SpO2 78%) with normal CO2 elimination (normal PCO2) represents the classic Type 1 respiratory failure pattern where oxygen diffusion fails but CO2 is still eliminated because CO2 is 20 times more diffusible than oxygen 1
• The respiratory rate of 22 breaths/minute with severe hypoxemia indicates compensatory tachypnea attempting to maintain oxygenation 2, 1
• Between 28-33% of patients with sepsis/infection meet ARDS criteria, making this the most common post-infectious respiratory complication 2

Why Other Options Are Incorrect

COPD (Option A) is excluded because:

• COPD patients typically present with hypercapnia (elevated PCO2) due to chronic CO2 retention, not normal PCO2 2
• A 38-year-old without prior respiratory history is too young for typical COPD presentation
• COPD exacerbations show Type 2 respiratory failure (elevated CO2), not isolated hypoxemia with normal ventilation 2

Drug overdose (Option B) is excluded because:

• Opioid or sedative overdose causes hypoventilation with elevated PCO2 and respiratory acidosis, not normal ABG parameters except PO2 3
• The patient would show decreased respiratory rate (<8 breaths/min), not tachypnea at 22 breaths/min 2
• No history of drug exposure is provided

Myasthenia gravis (Option C) is excluded because:

• Myasthenic crisis causes neuromuscular respiratory failure with hypoventilation and CO2 retention (elevated PCO2), not isolated hypoxemia 3
• The acute 5-day progression following infection doesn't match myasthenia presentation
• Myasthenia would show Type 2 respiratory failure with abnormal ventilation parameters

Pathophysiological Mechanism

ARDS causes severe hypoxemia through two primary mechanisms: 1

• Ventilation-perfusion (V/Q) mismatch: Blood perfuses areas of lung that are poorly ventilated due to alveolar inflammation and edema
• Intrapulmonary shunting: Blood flows past completely collapsed or fluid-filled alveoli without any gas exchange occurring 2, 1

The preserved CO2 elimination despite severe hypoxemia occurs because: 1

• CO2 diffuses 20 times more readily than oxygen across the alveolar-capillary membrane
• Even diseased alveoli can eliminate CO2 effectively while failing to oxygenate blood
• This creates the characteristic pattern of isolated severe hypoxemia with normal PCO2

Immediate Management Priorities

Oxygen therapy must be initiated immediately: 1

• Target SpO2 of 94-98% to prevent hypoxic brain injury
• The critically low PO2 of 5 kPa represents immediate life-threatening hypoxemia requiring urgent intervention 2
• Do not withhold oxygen due to theoretical CO2 retention concerns when PO2 is this critically low 1

Prepare for mechanical ventilation: 1, 4

• If oxygen therapy fails to achieve target saturation, intubation and positive-pressure ventilation will be required
• Lung-protective ventilation strategies should be employed once intubated 4

Obtain arterial blood gas analysis to confirm diagnosis and guide ventilatory support 1

Critical Pitfalls to Avoid

Do not delay treatment while obtaining chest X-ray: 1

• Radiographic changes in ARDS often lag behind physiological derangements by hours to days
• The clinical presentation with ABG findings is sufficient to initiate treatment
• Chest X-ray may be normal in up to 20% of early ARDS cases 2

Do not assume normal respiratory rate means adequate ventilation: 2

• Respiratory rate of 22 breaths/min with SpO2 78% indicates impending respiratory failure
• Hypoxemia with SpO2 <90% is a strong predictor of need for intensive care and mechanical ventilation 2

Recognize that hypoxemia at this severity (PO2 5 kPa) causes abrupt decreases in renal function and can lead to multi-organ dysfunction if not corrected urgently 2, 5